Cell-type specific gene expression occurs not only in the nucleus, but in mitochondria and plastids as well. Several differentiated plastid forms arise from undifferentiated proplastids, their differentiation being tightly coupled to the developmental stage of the surrounding cell. Posttranscriptional events within the plastid appear to be of primary importance in mediating plastid differentiation. The long term objective of this work is to elucidate mechanisms of communication between different genetic compartments. The more immediate goals are to evaluate several specific models of plastid posttranscriptional control and to determine the roles of two nuclear genes (identified by mutation) in plastid development. Experiments will focus on a set of four cotranscribed plastid genes that yield an elaborate set of overlapping RNAs. Proteins encoded by this gene cluster are either expressed coordinately or differentially, depending on the plastid type. Thus, although the four genes can be cotranscribed, their expression is uncoupled in response to certain developmental signals. Preliminary results suggest that expression of these genes may be regulated at several levels including transcription initiation, RNA processing, RNA stability, translation and protein turnover. Each of these potential mechanisms will be evaluated and further defined. Two nuclear mutations that prevent the stable accumulation of these plastid gene products will be used to assess the roles of specific nuclear genes in plastid development. One of the mutants is defective in the splicing of the multigene transcripts. The other mutant, having striking alterations in the morphology of its internal chloroplast membranes, will be used to define requirements for the stable insertion of large protein complexes into the membrane. This mutant arose in a Robertson's Mutator background, its mutation presumably caused by the insertion of a Mu -type transposon. The Mu tag will be used to isolate the mutant and normal alleles for further study.